The Role of YY1 in Prostate Cancer
Abstract
Our previous studies showed that CMV promoter-driven YY1 overexpression did not form any tumor in renalgraft studies. To repeat this experiment alternatively, we made a new vector with chicken-beta actin promoter and IVS(II) that support sustained and high YY1 expression. Our previous studies also showed that Pten-null prostate cells with siRNAs did not form any graft. We believe the cells have lost their stem/progenitor cell features. We thus made new batches of Pten-null clones that formed tumorigenic grafts in mice. We determined that residues 201-226 of YY1 interact with both Hdm2 and Ezh2. To distinguish YY1's regulation to these two proteins, we generated 5 YY1 mutants with alanines replacing the residues in this region. We compared the Hdm2- and Ezh2-interactions of wild type YY1 and these mutants. The preliminary results indicated that all these mutants lost their binding affinity to Hmd2, while some retained different degrees of interactions with Ezh2. We also observed the interaction of YY1 and Pten, which could be disrupted by p53, suggesting Pten and p53 compete in binding to YY1. Interestingly, YY1 overexpression negatively regulates the endogenous levels of Pten, suggesting an oncogenic or proliferative activity of YY1.
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 01, 2010
- Accession Number
- ADA529373
Entities
People
- Guangchao Sui
Organizations
- Wake Forest University